Neuroprotective effect of selective antegrade cerebral perfusion during prolonged deep hypothermic circulatory arrest: Cerebral metabolism evidence in a pig model

Neuroprotective effect of selective antegrade cerebral perfusion during prolonged deep hypothermic circulatory arrest: Cerebral metabolism evidence in a pig model
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长时间深低温停循环期间选择性顺行脑灌注的神经保护作用:猪模型中的脑代谢证据

DOI:
10.14744/anatoljcardiol.2017.7946
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发表时间:
2018-01-01
影响因子:
1.3
通讯作者:
Wu, Zhongkai
Wu, Zhongkai
中科院分区:
医学4区
文献类型:
--
作者:
Tang, Zhixian;Liang, Mengya;Wu, Zhongkai

文献摘要

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目的:本研究的目的是阐明脑损伤的机制,并评价选择性顺行性脑灌注(SACP)作为延长深度低温循环停搏(DHCA)的优越神经保护策略。方法:12头6 ~ 8周龄猪随机分为单独DHCA组(n=6)和DHCA + SACP组(n=6),温度18℃,持续80 min。采用免疫分析仪测定血清S100。用微透析分析仪测定脑透析液中葡萄糖、乳酸、丙酮酸、甘油和谷氨酸的浓度。结果:与DHCA组在T4(复温60 min后)出现峰值相比,SACP组在整个研究过程中血清S100明显降低。DHCA组乳酸、甘油、谷氨酸水平显著升高,乳酸/丙酮酸比值显著升高,葡萄糖水平显著降低。这些微透析变量在SACP组中仅显示出微小的变化。DHCA组再灌注时脑乳酸与颅内压呈正相关。而SACP组细胞凋亡指数和C-FOS蛋白水平较低。结论:代谢功能障碍参与脑损伤的发生机制。SACP对于轻度和长期DHCA都是一种优越的神经保护策略。
Objective: The aim of this study was to elucidate the mechanism of cerebral injury and to evaluate selective antegrade cerebral perfusion (SACP) as a superior neuroprotective strategy for prolonged deep hypothermic circulatory arrest (DHCA). Methods: Twelve pigs (6–8-week old) were randomly assigned to DHCA alone (n=6) and DHCA with SACP (n=6) at 18°C for 80 min groups. Serum S100 was determined using an immunoassay analyzer. The concentrations of cerebral dialysate glucose, lactate, pyruvate, glycerol, and glutamate were measured using a microdialysis analyzer. Results: Compared with a peak at T4 (after 60 min of rewarming) in the DHCA group, the serum S100 in the SACP group was significantly lower throughout the study. The DHCA group was susceptible to significant increases in the levels of lactate, glycerol, and glutamate and the ratio of lactate/pyruvate as well as decreases in the level of glucose. These microdialysis variables showed only minor changes in the SACP group. There was a positive correlation between cerebral lactate and intracranial pressure during reperfusion in the DHCA group. However, the apoptosis index and C-FOS protein levels were lower in the SACP group. Conclusion: Metabolic dysfunction is involved in the mechanism of cerebral injury. SACP is a superior neuroprotective strategy for both mild and prolonged DHCA.